Heme metabolism and its relationship to non-pathological transient porphyria in the fetus and newborn will continue to be pursued. The major goals of this proposal will be to determine the biochemical basis for the accumulation of porphyrin metabolites during fetal development. To meet this goal a primary objective of the investigation will be to establish the enzyme ALA synthetase level and prophyrin metabolite levels during fetal development. Characterization of ALA synthetase from fetal liver and from livers of adult guinea pigs induced with 3,5 dicarbethoxy-1,4-dihydro collidine will be pursued. The concentration of various metabolites that accumulate during fetal development will be determined at various stages of development in the fetus of sheep, guinea pigs and other mammals. Determination of the tissue of origin for fetal porphyrin metabolites will be necessary. As we explore the mechanism for excess Uroporphyrin 1 production in the fetus it will be important to estimate the life span of fetal erythrocytes so that we can relate this to erythropoietic activity and hepatic activity as possible sources of porphyrin production.